RESPIRATORY SYSTEM Fibrosis = decrease in compliance and hardening. Lateral traction increased, hard to expand ● 100% O2 in a shunt?

nd hardening. Lateral traction increased, hard to expand ● 100% O2 in a shunt? Hb carries most O2 and is almost fully saturated already; 100% O2
Intraplural P (Pip)– made less negative (more +) by ↓ lung elasticity. lungs would result in a small amount of O2 to Hb, contributes nothing to shunted venous
Intrapulmonary pressure = alveolar pressure (Palv) Bronchitis= inflammation of bronchioles but have the same compliance as a regular person blood, PO2 would rise, but content would change only slightly
TPP (trans pulmonary pressure) = distending pressure (hold open) TPP= P(alv)– P(ip) @ high altitudes - ↓O2 (hypoxia) so ↑ Ventilation ↓pCO2 (alv) ● Diffusion Impairment: between alveoli and capillaries; alveolar gas and capillary blood do
Airway Structure: trachea-bronchi-bronchioles-elastin+some cartilage in framework gives - Airflow ventilation Pgas = F% x Ptotal not equilibrate; PaO2 falls and PAO2 remains normal; caused by Diffuse Interstitial
elastic properties and recoil force to keep airways open, but can collapse. Top ↓V,perf,C ↑V/Q, >1 ↓Q ↑TPP ↑O2 fibrosis, asbestosis, fluid build up/thickening of alveolar walls caused pneumonia; can
Inspiration: external intercoastals up & out, diaphragm pulls down. IP space remains the Bottom ↑V,perf,C ↓V/Q, <1 ↑Q ↓TPP ↓CO2 give 100% O2 to try and push O2 into perfusion
same (closed container) (P1V1 = P2V2) - As you go up the lung V/Q goes up, bc Q goes down rapidly ● Elite athletes – huge CO – short transit time of blood through capillaries – blood not fully
Pressure changes during inspiration – pre-inspiration TPP = 0 - -5 = +5; during -2 - -8 = +6; - Q blocked – alv air is comp of inspired air. oxygenated – PcO2 down and widened Δ(A-aO2)
end inspiration 0 - -9 =+9; mid expiration 2 - -4 = +6 Fick’s Law of Diffusion = Vgasdiffused = DxSAx(P1-P2)/T D=diffusability, SA=surface area, ● SUMMARY: Hypoxemia causes: decreased PlO2, Hypoventilation, Ventilation/Perfusion
Expiration – passive, no muscle needed. Palv > Pout, so air flows out. Everything returns to T=distance mismatch, Shunt right-left, Diffusion impairment
original dimensions. O2 diffuses through surfactant layer, alveolar epithelium, interstitium, pulmonary capillary ● Gravity: gradient in ventilation+perfusion (low apex, high bottom); gradient for perfusion
Pneumothorax – collapsed lung; Patm>Pip normally; hole in IP space cause Pip=Patm; chest epithelium, plasma, and RBC membrane is steeper (high apex, low bottom), Va/Q=0 poor ventilation, Poor perfusion Va/Q
wall expands outward, lung recoils inward; negative pressure in IP space made less negative Solubility – CO2 much higher, small pressure difference; opposite for O2; lots of CO2 after =infinity
at FRC decreasing inward recoil force of lung – age, emphysema alveolar gas exchange (bicarb, pH balance) TRANSPORT OF O2 AND CO2 O2 40mmhg->100 CO2 46mmHg->40mmHg
Compliance C = ΔV/TPP (Δtpp needed to ↑ lung volume.) ↑C easier to expand lungs at any Perfusion limited = gas exchange dependent on blood flow; 0.75 second in capillary ~2-3 21% O2, 79% N2, .02-.03% co2 1atm=760mmhg PH2O @37C: 47mmHg
given P. (↑blood Vol, edema, hyaline membrane disease=↓C). stronger recoil forces = lower alveoli, O2 equilibrates in <0.3 sec; x2 blood flow, perfusion time 0.375s, all blood would still Gas phase-pp proportional to conc. Po2=Pb x Fo2. Liquid phase-pp at which liquid neither
compliance. Emphysema & age ↑ C equilibrate gives up nor takes up the gas.
Elasticity (collagen and elastin) & Surface tension contribute to lung recoil. NOT diffusion limited = blood would not equilibrate during time it is in alveoli - Henry’s law - amount of gas dissolved in art blood = Pgas x Solub Coef
Surfactant: phosphatidylcholine + surfactant proteins (spABCD), 26 weeks after gestation, Hypoxemia = low PaO2 Solubility coeff= O2 ( .003) Co2 (.075), N2 (.0017). ↑T=↓solub.
secreted by alveolar type2cells Decrease in PO2; high altitude %O2 stays same but PO2↓, breath more or hypoxemia Plasma & blood same PO2. More O2 in blood bc is bound to Hb.
La Places Law: P=2T/radius T=tension P= required to keep alveoli open. ● Hypoventilation; ↓VA, VO2 same or increased; PAO2↓ and PaO2↓; usually happens 15g Hb/100 mL of blood, 1 g can bind 1.34 mL = 21 mL O2 bound
Infant Respiratory Distress – lowers compliance, born without surfactant, lungs usually peripheral to lungs; neuromuscular diorders, narcotics, lungs normal >↑ altitudes, ↓PO2 - ↓ ability of Hb to be sat. (~60-80 mmHg)
collapse; synthetic surfactant, treat mom with cortisol, CPAP, mechanical ventilation ● Gravity: More negative intrapleural pressure (Pip) at lung apex; gradient from top to anemic - ↓ amount of Hb hence ↓amount of O2 in the blood. Saturation is not affected, PO2
Resistance: 20-25% in upper nasal. Greatest resistance in bronchial tree is medium sized bottom; gradient in alveolar distending pressure; A=alveolar, a=arterial is the same.
th
bronchiole 7 generation. Airways in parallel. 1/Rt. Affected by TPP, and lateral traction. ● APEX = alveoli more distended, larger alveoli, less compliant In lungs-HbO2 stronger acid than deoxy, gives up proton, combining with hco-3 going

Palv −Patm ● Inspiration: ↓Pip, greatest volume increase in most compliant alveoli/bottom opposite direction. In tissues Haldane affect, deoxy picks up H+ produced from dissociated
● Every cm. above heart = 1 cm H2O decrease in hydrostatic pressure bicarb. For every mmol of O2 used, 0.7 mmol Co2 produced. lungs & kidneys play role in acid
● ↓P – less distended - ↓r – increase Resistance - ↓Q; ↓Q at apex vs. ↑Q at bottom of lung base regulation.
Poiseullie eqt: F= = ΔP/R. R α viscocity of air, -p50 of fetal is 15-20mmhg
● Gradient in perfusion, gradient in ventilation = both low at apex, high at bottom

R ● Perfusion = V/Q; steeper at apex; more ventilation than blood flow

● Shunt: Va/Q=0; equilibrate to near mixed venous blood
● Dead space: Va/Q ~infinity; equilibrate to near inspired
- CO monoxide higher affinity than O2 for Hb (240x), bound to Hb prevents O2 transport - its
produced by degradation of porphyrin ring. Shifts curve all the way to the Left. ↓ amount of
O2 delivered to the tissues.
length of airway, and 1/r^4
● Va/Q and arterial blood: ↑Va/Q blood volume <↓Va/Q blood volume; - CO2 – In both blood & plasma: dissolved (10%), as bicarbonate (60%)& carbamino (30%) …
**Dynamic Compression: interior + abs: TPP between alveoli and intraplueral space is
● APEX - ↑Va/Q - ↑PO2 – ↓blood volume/min drain % = how much contribute to gas exchange. The lower the saturation of Hb w O2, the larger
always positive. TPP becomes neg = Pip>Palv, overcomes lateral tension. Collapse less likely
● Bottom: ↓Va/Q - ↓PO2 - ↑blood volume/min drain the CO2 content for a given PCO2 ← Haldane effect.
at ↑ lung volumes(low Pip). Max flow ↓ w/ lung volume.
Ve = minute ventilation (about 5400 mL/min) Ve = Vt x f ● If ↑Va/Q =↓Va/Q, PO2 in final mixed blood lower than expected; average O2 contents, pH Regulation : pH = -log[H+]
f = frequency (breaths/min) Va = (Vt-Vd-anat) x f NOT their partial pressures than convert to partial pressure; CO2 – content and partial ● Pancrease, blood – 7.35-7.45; gastric HCl 1; duodenum 7.5; H2SO4, H3PO4, ketone
pressure relatively linear bodies, lactic acid. Main source of acid is products of metabolism. Greatest proton
Vd-anat = anatomic dead space; air that remains in conducting airways (about 150 mL)
● Small amount of O2 added from high Va/Q regions cannot compensate for deficit from producer is Co2 produced from breakdown of carbs and FA.
VA = alveolar volume ventilation (about 3600 mL/min)
low Va/Q regions ● Other buffers: phosphate, bone calcium phosphate during chronic acidosis. Final role is
Vd-alv = alveolar dead volume. Pathological. No exchange w/ blood
Va/Q heterogeneity in lungs: A=alveolar, a=arterial through the kidney to expel protons to restore normal Co2/HCO3 relationship.
Can effectively ignore Vd-alv except for; Vd-physiologic = Vd-anat + Vd-alv
Lung Volumes = 4-7L ● Asses Δ(A-aO2); should be no difference between PlO2 and PaO2 BUT-low V/Q regions ● Respiratory Acidosis – caused by hypoventilate/impaired ability to breath, acidic pH;
have lower PlO2; ↓PaO2 relative to mean PAO2; widening of Δ(A-aO2) inadequate ventilation, ↑CO2, ↑ H; can’t compensate by hyperventilating. Shift to right.
Can’t determine FRC, RV, TLC with standard tools/spirometer
● Ventilation/Perfusion mismatching: ● Metabolic acidosis – body loses alkaline, fluid left is acidic; diabetic 1, diarrhea (flush
Vt = tidal volume = single respiration ~500 mL. v. in & out in normal cycle. ↑ w/ exercise.
● Normal: Pulmonary Q – well ventilated alveoli – efficient exchange of gases HCO3-), failure of kidney to expel H+; respiratory compensation increases ventilation to
IRV = inspiratory reserve volume = forced respiratory effort ~2.5-3L
● Poor ventilation: ↑CO2, ↓O2; high ventilation: ↓CO2, ↑O2 – vasodilation sends blood expel more CO2.
ERV = expiratory reserve volume = forcedl expiration ~1.5L
● PaO2<PAO2 = natural shunts, mismatch of ventilation and Q in various parts of lungs ● Respiratory alkalosis: caused by hyperventilate; (↑O2, ↓ pCO2), ↓ H+. shift to left.
VC = Vital capacity = max insp. Followed by max exp.
● Q=5L/min normally, VA ~4L/min, VA/Q=0.8 ● Metabolic alkalosis; ↑loss of acid, ↑vomiting; ingest alkali – result in loss of H+
RV = residual volume = what’s left after VC (1.5)
FRC = functional residual capacity = end of expiration. Recoil forces =. ● Pulmonary Disease can produce significant mismatch; widened Δ(A-aO2) ; note enough BLOOD –RBC: energy derived from anaerobic glycolysis, no O2 used
ventilation in a well perfused area Hematocrit = B/A 45% RBC, plasma 55%
FVC =total volume expired. should be able to get 80% of air out in 1 second in healthy
airways; Vital Capacity = VT + IRV + ERV = VC breath all in, slowly all out. FEC= volume ● Shunts: Right to left; extreme V/Q mismatch; arterial blood mixedPlasma;
w/ bloodH2O
that91%,
did solutes
not 2%, proteins 7%; albumin = single protein/carriers 55%, globulin mix of a, B, gamma 43%,
expired in 1 sec. exchange gases in lung (mixed venous blood); some are normal – returning bronchial fibrinogen 2-3%
Emphysema: ↑FRC ↑C, ↓FVC, ↓V/Q, easy to inhale, hard to exhale circulation to left heart via pulmonary veins and returning coronary venous blood to left Buffy coat= platelets + WBC’s: Defense: WBC’s granulocytes – neutrophils 55%, basophils
ventricle via thesbian veins ● RBC = no nucleus, no mito, no ribosomes; just pack lots of Hb; Hb no more than 2 um in RBC
- Equilibration is purely perfusion (flow) dependent. Test w/ FEV/FVC is less than 0.8, 0.8 in
● Congenital Heart Disease – atrial septal defects, patent foramen ovale helps diffusion; spherical cell Is not favorable – too far for O2 to diffuse in/out, will tear in
normal person. Loss of elastin and collagen fibers. In COPD, this ratio is much lower. In
● Pulmonary Disease – can lead to significant shunts = cor pulmonale capillaries; Spherocytosis=RBCs spherical, leads to anemia; RBC plasma
chronic bronchitis, this is due to the inflammation and severe narrowing of the airways. In membrane=phosphor/glycolipids, glycophorin A, spectrin (lack of causes spherical), actin;
emphysema, it is because there is little elastic support and the airways are easily collapsed. ATP required for RBC to keep shape, no ATP will cause ruffling & crenated; deficit in spectrin
 = spherocytosis; NA/K+ATPase helps keep Ca2+ out, RBC deforms if high [Ca2+]→spikes stored in Scavenger macrophage then given to transferin ; Porphyrin – bilirubin, albumin a-2-globulin antithrombin III: binds & inhibits thrombin & activated CF IX, X, XI, XII.
echinocytes. Hence ATP need. Not insulin dependant (no receptors) binds to bilirubin to excrete it as waste in liver. Bilirubin yellow builds up bc it not removed enhanced by heparin! Thrombin binds to thrombomodulin, loses procoagulant activity,
● MetHb Reductase: reduces Fe3+ to Fe2+; ferric to ferrous; uses NADH derived from from body. Jaundice,iteric. activates protein C. Protein C & S inhibits CF VIII & V. Thrombin directly activates VIIIa & Va
glycolysis; could have pathology if missing metHb reducatse. Denatured methhb forms REGULATION - ↑ depth of respiration by: 1) ↑f of impulse, 2)recruitment3)longer duration but also inactivates them indirectly via Protein C/S. Tissue Factor Pathway Inhibitor: inhibits
aggregates called Heinz bodies, precipitate and shorten life of cell. NADH produced from of burst. First two increase minute V, but not 3 because equaled by expiration. VIIa. Limits clotting
hexose monophosphate shunt [nadph drives reduction of GSSG]. Central Pattern Generator – tell brain to shut the in/ex cycle – located in the Fibrinolysis: Plasminogen→Plasmin, present in circulation as an inactive proenzyme
● Reduced Glutathione (GSH): GSH protects cell membrane and Hb against oxidants like brainstem/medulla plasminogen. Plasmin is able to degrade both fibrin and fibrinogen, helps remodel and
H2O2; GSH uses oxidative species before Hb is damage; deficiency in G6PD causes hemolytic C3-C5 –brainstem to phrenic neuron (motor neuron) → diaphragm break down clot (healing)
anemia; anaerobic glycolysis = 90% RBC ATP. T1-T7 – from brainstem to motor neuron → intercostals. BODY TEMPERATURE age, time of day, mens.cycle, exercise change it
● Rapoport shunt: produces DPG, ↓ o2 affinity for Hb Lumbar 1-5 – abdominals in forced expiration Humans are Homeotherms: wanna keep a narrow range of temp for processes
● Marrow Precursor Cells: 1) pluripotential stem cells that give rise to Cut above brainstem – unconscious but you can cyclic breath Eliminate heat through convection (liquid/blood, major) conduction (contacting cells)
RBCs/platelets/monocytes/granulocytes/lymphocytes 2)Committed stem cells that develop Cut at C3 - can’t breath, ventilator, insp muscle not fxn Forms of heat transfer: radiation, conduction, convection (dependent on heat transfer
from pluripotential cells and give rise to only one type of blood cells Cut at T# – affects forced exhale, below FRC. capacity), evaporation
● Takes place in bone marrow for adults; yolk sac, liver, spleen for infants - Augmenting Pattern - during inhalation, ↑ firing as it goes ↑ freq and then it stops., recruits Peripheral thermoreceptors all over skin. Coarse temperature discrimination (non-acral, e.g.
● Pluripotent cells have ability to differentiate into many cells; stem cells in bone marrow, motor neurons trunk/limbs) and fine temp. discrimination (acral skin, e.g. face, lips, finger)
chemo will kill some pluripotent stem cells; Stem cells that form into RBC’s will make Hb DRG (A)– inspiration neurons (diaphragm & intercostals); sends signal to VRG during Ion channels (TRP family) open when it experiences the temperature it detects.
until they leave the bone marrow and enter circulation inspiration to stop firing. Hering Bruer-pulmonary stretch receptors (↑ inspiration, ↑ firing central receptors: (preoptic area & hypothalamus), ONLY WARMTH SENSITIVE.
● Reticulocytes = last for 2 days: look at reticulocyte index measure (2/100=2% normal) to of vagal to A) Thermoreceptor integration: if skin says you’re in warm environment, and core temp drops,
check for low RBC count (2 days/50 days = 4% problem). has reticulum RNA and ribosomes. VRG – forced exhalation goes to Pre- Botzinger Complex (pacemakers) – talks to DRG to metabolic rate only increases a bit. If skin cold, increases more aggressively. EFFECTORS:
Will boot before becoming RBC. No division needed to become RBC. stimulate inhalation after the inhibition by “switch off” (C) cutaneous circulation(SNS withdraw in acral skin to use plexi, stimulate non-acral skin to
● # of rbc controlled by production not distruction. PontineRG – pneumatonic center –innervates DRG – early cut off of respiration vasodilate. Reverse with noradrenergic), sweat glands (stimulate w/ SNS Ach. releases
● Erythriopoieten is the hormone in the kidneys in response to low oxygen that is released to - cut vagus or btw medulla and PonRG – deeper breaths and ↓ freq. cut both = mess kallikrein-> bradykinin vasodilates), muscle/shiver, Brown adipose tissue: β3 α1 sense NE in
stimulate RBC formation; ion delivery system; give rise to mature RBC. Alt, hemorrhage, - ↑pCO2, ↑H+,↓pO2 = trigger to ↑Vent :: ↓pCO2 = ↓Vent cold>cAMP>kinase>lipase(turns triglyceride to FA) FA enters outer mito., acts on
increased destruction of rbc. - ↑pCO2 is more effective in ↑ Vent. than ↓pO2, more sensi to CO2 UCP(uncoupling protein), dissipates H+ gradient and makes heat. T4 also released,
● Normoblast = undergo 3-5 divisions and become increasingly differentiated, produces - Central R – @ medulla, Stimulated by ↑pCO2 (↑H+) and ↓pH of CSF :: monitor acidity of CSF. converted to T3 by 5’deiodinase(by α1) to act on UCP. O2 DEPENDANT!!
reticulocyte; have cell surface receptors for transferrin. Hb sysnthesis occurs. Nucleus and ::: NOT activated by ↓ arterial pH pre hypoxia (BBB doesn’t allow H+ to cross over). Fever: immune cells release pyrogens and cytokines that cross BBB and endothelial brain
mit extruded producing reticulocyte (contains rna, and ribosomes. - Peripheral R - @ carotid and aortic bodies, respond to changes in H+ and pO2 :: Main tissue makes cyclooxygenase make prostaglandin E2, which inhibit heat sensors in
● Fe2+ deficiency = most common cause of anemia sensor is Glomus :: ↓pO2 and ↑H+ metabolic acidosis – K ch get blocked (caused depo) , VG hypothalamus, so you start swinging temp. Fever may ↑T-lymphocyte proliferation
● Macrophage phagocytosis old RBC’s; can retain Fe in inflammatory disease Ca Ch open promote release of NTs dopamine. 3) Vesicle fusion, and 4) signal transduction.
● Haptoglobin:. some RBCs lysed in circulation, haptoglobin levels indicative of a hemolytic CUT – no longer respond to arterial pO2, but Central R can detect C02 still. pCO2 remains
event, haptoglobin levels will be down; hemolytic event = lysing of RBC, i.e. bacterial events unchanged. ↑H→↑Tidal Vol & freq

receptors trigger for pain, ⇑ sympathetic firing. Both prevent blood loss while clotting occurs
| Hemopexin binds heme from MetHb in intravascular hemolysis HEMOSTASIS 1) Vasoconstriction - Myogenic vasospasm: in SM of vessel. Neurogenic
● Anemia: low RBC count/low O2 (low Hb); 1)not making enough RBCs = hypoproliferative
(low [Fe2+], blood loss, prolonged inflammation, renal diasease.) 2) Breaking RBC down too (20 mins). Humoral Responses: released locally to vasoconstrict (hours). Form platelets in
fast (hemolytic events, bone marrow destruction/thalassemia); pernicious anemia = low “release rxn”. Serotonin,ThromboxaneA2(derived from pl), ProGlanF, ADP
B12 due to lack of absorption need; intrinsic factor=lowered, causes B12 to be lowered); 2) Form platelet plug: contact of blood with CT. Platelets don’t stick to endothelial, bind to
examples include hereditary spherocytosis [spherical], sickle cell anemia, hereditary G6P subendothelial collagen → platelet adhesion. “Release Reaction”, release Ca, serotonin &
deficiency. (reduces ability of oxidation. ADP. Platelet Aggregation: binding of platelet to platelet. High ADP & TA2 help clumping.
● B12 & folic acid needed for biosynth, prolif occurs in marrow. Platelet membrane phospholipid acted on by enzymes to produce TA2, which promotes
● Increase # RBCs: 1)Increase size of erythroid marrow compartment/total # of erythrocyte aggregation (humoral vasoconstrictor). Prostacyclin (PGI2): inhibitor of aggregation in
precursors 2)Increase in rate of maturation of erythrocyte precursors surround endothelial cells, prevents platelet aggregation from extending away from injury.
● Hemoglobin Synthesis: globin in ribosome. heme = porphyrin ring containing Fe2+;, Cyclo-oxygenase: enzyme involved in producing TA2. Aspirin acetylates & inactivates this
mitochondria make heme iron comes from transferrin. ( degraded RBC, body stores, & enzyme irreversibly, ↑bleeding. Von Willebrand Factor: bind onto subendothelial collagen,
dietary from GI) storage form contains of metal ion bound to ferritin or hemosiderin. required for platelets to bind to collagen (adhesion), required to maintain function of CF VIII.
● Blood Typing: Type A has anti-B Abs, Type B has anti-A Abs, type AB has no Abs, type O has Constriction & plug= primary hemostasis
all Abs; O=universal donor, AB =universal recipient; Abs don’t go with transfusion; Rh- mom Hemophilia: can’t coagulate, no secondary., Type A: CF8 (most common), Type B: CF9,
and Rh+ baby=first baby ok, second baby not because mom has Anti-D Abs = Christmas.
erythroblastosis fetalis; treat with injection of Anti-D Abs into mom (RHOGAN) > With Ca, prothrombin → thrombin by thromboplastins released from damaged
● Hb Fate: see pic.; RBC broken into AA’s and heme; AA’s recycled; Heme breaks into tissues/platelets release rxn. Thrombrin activates Fibrinogen → fibrin clot. Held together by
porphyrin and Fe2+; porphyrin broken into biliribun and CO (CO exhaled), biliribun to weak non-covalent forces then crosslink covalent bonds (Fibrin Stabilizing Factor, CF XIII).
albumin to liver and conjugated with glucoronic acid to form bile, excreted to gut and feces - Intrinsic Pathway. – factors found in blood. Contact-activation system. XIII starts clotting
(jaundice =build up of bile); Fe2+ bound to plasma transferrin and goes to bone marrow cascade, amplifies signal pathway. Activates prothrombin→thrombin (which activates
@ tissues: O2 out, HCO3 out, Cl in, H20 in, CO2 into cell fibrinogen). Platelet phospolipid (PF3) is template for 8 & 9 to activate X.
- Kidney regulation–monitor production rate,↓pO2, ↑erythropoietin/hb - Extrinsic Pathway. Req from tissue trauma → Tissue Thromboplastin (protein +
α and β globin are synthesized on ribosomes in cytosol of normoblast. The prophyrin group phospholipid) CF VII, 7 →activates CX to activate prothrombin. VIIa activates X with Ca and
of heme is synthesized in the mitochondria of this cell phospholipid – positive feedback Xa is able to activate more VII. Calcium- -carboxyglutamic
Intravascular Hemolysis- destruction of freely circulating blood cells, due to transfusion acid: critical for Ca binding to CFs. Vitamin K requ for carboxylation to form y-
reactions or Rh-incompatibility, decrease hapatoglobin levels carboxyglutamic acid from glu. No Vit K →no y-carboxyglutamic acid →no Ca binding
Extravascular hemolysis -RBC Lysis (@spleen) . in free circulation→ Hb – dimers bind to factors→ no coagulation. Coumarin,Warfarin (anti-coagulant): blocks enzymatic addition of
hepatoglobin - @ reticulo-endothilial (liver) lysed to form aa (↓hapto – Hb in urine); Fe – carboxylates.: